Lp(a) is not uniform (Varies greatly in size and density) so I don't know how this method would separate Lp(a) from LDL.

Owen R. Fonorow, Orthomolecular NaturopathMy statements have not been evaluated by the Food and Drug Administration. Any product mentioned is not intended to diagnose, treat, cure or prevent any disease.”

Yes, I also think it isn't possible to separate. But I've asked Roche (Prof. von Eckardstein) - they measure nmol - and Ganzimmun - they measure g/l with nelometer - what they think about it. I'd like to see their answer and I'll report.

I got an answer from Prof. Eckardstein. He says, that nephelometry isn't per se problematic. The basic problem is the difficult standardization of lp(a) measurement. According to Prof. Eckardstein a good summary of this problem can be found at https://www.ncbi.nim.nih.gov/pubmed/26637278.It appears to me, that I took up a very interesting (and important) question.

Today I had a telephone call with Prof. Scharnagl, Medical University Graz. He also said that the basic problem is the difficult standardization of lp(a) measurement. According to Prof. Scharnagl, it does not have to do with the separation of LDL. Lp(a) can be distinguished from this. The reason for the problem is the repetitive kringle structure of apo(a) protein.OK. But now I don't know furthermore which of my lab values are correct.

Although from what you sent me - the nmol/l is probably accurate and thus elevated. And no matter, taking Lp(a) binding inhibitors is warranted, and over time, I suspect the Lp(a) will decline.

Owen R. Fonorow, Orthomolecular NaturopathMy statements have not been evaluated by the Food and Drug Administration. Any product mentioned is not intended to diagnose, treat, cure or prevent any disease.”

Thank you, Owen. I see that too. And I'll continue to report at the forum. To provide complete information, the article from Prof. von Eckardstein: https://academic.oup.com/eurheartj/arti ... oprotein-a (I hope it's correct)But take into consideration, it's school medicine.

You could Ask your Good Professor when testing for levels of LP(a) what type of reagent they are using? If he says Glycerol.Then see if they ever tried using L-Proline as a reagent?A L-proline reagent causes LP(a) to separate from other lipoproteins and cluster and yield’s more accurate results especially when using the nephelometer. Which is a light diffusion method of measuring size and quantity of an object.

To steal ideas from one person is plagiarism. To steal from many isresearch!

It seems to me, that my post is of great interest. More than 6.000 klicks within 9 months. I hope, that it is helpful for you. Furthermore I'm sure, my lp(a) will decline with PT. And I'll report. But much more important, after my heart attack one year ago the damaged part of my heart muscle has begun to work again. No angina. No problems. And I'm fit. Every day 1 to 2 hours nordic walking, muscle training and riding a bike, although I'm 70 years old - sorry, young. And I learned, I can all if I believe it.

Johnwen wrote:Hate to sound like a broken record on the subject of Thyroid.When it comes to LP(a) there seems to be a connection!I let these links tell the story! There’s a lot more of these out there!

Just perhaps these inherited ideas are actually the results of a under active thyroid. Since if your at the high end of the lab test your already in the danger zone of a failing thyroid! However most doc’s will just see your in range and do nothing about it. Then they’ll send you on your way with a script for statins, which only will make matters worst! Then they’ll blame high cholesterol for all your problems! When the real problem is at the end of their pen!!

I've read David Brownstein's book "Overcoming Thyroid Disorders". He says: "I have found that a large percentage of individuals with elevated cholesterol levels have thyroid and other hormonal imbalances present (page 26)."And I remembered the post from Johnwen. If this also applies to Lp(a), I do not understand the connection. According to Linus Pauling and Matthias Rath Lp(a) is a surrogate for ascorbate. They said: "We now suggest a broader role of Lp(a) in tissue maintenance and repair. In brief, we propose that Lp(a) is a late member in the chain responses to cellular damage.Its role under physiological and parhophysiological conditions would be the attempt to reconstitute cellular and extracellular damage."

I would like to know why there could be a connection to thyroid function. Does the thyroid take away vitamin C? I don't know, if all individuals with hypothyroidism have elevated Lp(a).

From the meeting with Dr. Rath in Sept. 2017 in Leimen/Germany I have taken with me the german version of the article about lp(a) and arteriosclerosis in transgenic mice. And I have read it again. It is very interesting. And it shows and proves, cholesterol isn't the culprit. With PT we are on the right way. I think, that you know the study from Dr. Rath. If not, here is the link to the orginal english version: ajcd.us/files/ajcd0007056.pdfOtherwise, it is worth to read the study again.

Frodo wrote:It seems to me, that my post is of great interest. More than 6.000 klicks within 9 months. I hope, that it is helpful for you. Furthermore I'm sure, my lp(a) will decline with PT. And I'll report. But much more important, after my heart attack one year ago the damaged part of my heart muscle has begun to work again. No angina. No problems. And I'm fit. Every day 1 to 2 hours nordic walking, muscle training and riding a bike, although I'm 70 years old - sorry, young. And I learned, I can all if I believe it.

Thank you. Another anecdote for our "collection"

As far as the connection between thyroid, LDL and Lp(a). It is my understanding that Lp(a) *IS* LDL cholesterol, but that a new surface has been attached to the lipoprotein, made up of apo(a) - thus Lp(a). The University of Chicago found, after Pauling died, that the apo(a) binds to LDL via proline binding sites. I am not chemist and do not pretend to be one on the Internet, but it seems the same logic Pauling used to increase lysine in the blood (knowing Lp(a) bindings sites are what sticks to collagen residues on the arteries) applies, and that increasing proline might interfere with the production of Lp(a) in the liver.

Owen R. Fonorow, Orthomolecular NaturopathMy statements have not been evaluated by the Food and Drug Administration. Any product mentioned is not intended to diagnose, treat, cure or prevent any disease.”